Han Guang-Tao, Cai Wei-Song, Zhang Yu-Biao, Zhou Si-Qi, He Bin, Li Hao-Huan
Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Curr Med Sci. 2021 Feb;41(1):100-107. doi: 10.1007/s11596-020-2248-3. Epub 2021 Feb 13.
Osteoarthritis (OA) is a degenerative disease characterized by matrix degradation and cell death leading to a gradual loss of articular cartilage integrity. As a bacterial synthesis of quinine, pyrroloquinoline quinone (PQQ) is a strong redox cofactor with a variety of biological benefits, including antioxidant, anti-inflammation-induced mitochondrial metabolism regulation. This study was designed to investigate the effect of PQQ on TNF-α-induced mitochondrial damage in chondrocytes. Chondrocytes isolated from C57BL/6 mice were exposed to TNF-α 50 ng/mL, TNF-α 50 ng/mL + PQQ 10 µmol/L for 24 h. Then, morphological study, functional study and mechanism study were taken. The results revealed TNF-α-induced chondrocyte mitochondrion damage could be reduced by application of PQQ, evidenced by elevated number of mitochondria, well-kept mtDNA integrity, preserved ATP level, reestablished mitochondrial membrane potential, and prevented mitochondrial function. The present work strongly suggests that the mitochondrion is an important target for OA chondrocyte damage induced by TNF-α and the PQQ protection from this damage ameliorates mitochondrial dysfunction induced by TNF-α. PQQ might be a potential chemical for OA intervention.
骨关节炎（OA）是一种退行性疾病，其特征是基质降解和细胞死亡，导致关节软骨完整性逐渐丧失。作为一种细菌合成的奎宁，吡咯喹啉醌（PQQ）是一种强大的氧化还原辅因子，具有多种生物学益处，包括抗氧化、抗炎诱导的线粒体代谢调节。本研究旨在探讨PQQ对肿瘤坏死因子-α（TNF-α）诱导的软骨细胞线粒体损伤的影响。从C57BL/6小鼠分离的软骨细胞分别暴露于50 ng/mL TNF-α、50 ng/mL TNF-α + 10 µmol/L PQQ中24小时。然后，进行形态学研究、功能研究和机制研究。结果显示，应用PQQ可减少TNF-α诱导的软骨细胞线粒体损伤，表现为线粒体数量增加、线粒体DNA完整性良好、ATP水平保持、线粒体膜电位恢复以及线粒体功能得到保护。目前的工作强烈表明，线粒体是TNF-α诱导的OA软骨细胞损伤的重要靶点，PQQ对这种损伤的保护作用可改善TNF-α诱导的线粒体功能障碍。PQQ可能是一种用于OA干预的潜在化学物质。
